Biology of Sport, Vol. 26 No3, 2009
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ANTIOXIDANT CAPACITY AND PHYSICAL EXERCISE
A. Marciniak1, J. Brzeszczyńska2, K. Gwoździński3, A. Jegier1
1
Dept. of Sport Medicine, Medical University of Lodz, Poland; 2School of Life
Sciences, Sport and Exercise Science, Heriot-Watt University, Edinburgh, United
Kingdom; 3Dept. of Biophysics, University of Lodz, Poland
Abstract. The aim of this article is a presentation of current knowledge regarding
the changes of plasma antioxidant capacity observed in response to physical
exercise. Human body created the enzymatic and non-enzymatic systems, which
play a protective role in the harmful impact of free radicals. Those two systems
constitute what is known as the plasma total antioxidant capacity. The amount of
reactive oxygen species (ROS) and reactive nitrogen species (NOS) in
combination with oxidation processes increases in some tissues during
physiological response to physical exercise. These changes are observed after
single bout of exercise as well as after regular training. The response of human
body to physical exercise can be analysed using various models of exercise test.
Application of repeated type of exhaustion allows for characterizing the ability of
human body to adjust to the increased energy loss and increased oxygen
consumption. This article presents the characteristics of components of plasma
antioxidant capacity, the mechanisms of free radicals production and their role in
human body. It discusses also the currently used methods of detecting changes in
total antioxidant capacity and its individual elements in response to single bout of
exercise and regular training. It presents the review of literature about research
performed in groups of both regularly training and low exercise activity
individuals as well as in group of healthy subjects and patients with circulation
diseases.
(Biol.Sport 26:197-213, 2009)
Key words: Antioxidant capacity – Exercise - Free radicals - Oxidative stress
1.1 Characteristics of antioxidant capacity in cells and in plasma
The use of oxygen for breathing by living organisms is connected with
production of its reactive forms, the so-called free radicals. In order to protect the
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Reprint request to: Dr Aleksandra Marciniak, Dept. of Sport Medicine, Medical University
of Lodz, pl. Hallera 1, 90-647 Łodz, Poland; Tel.: (0-42) 639 32 15; Fax (0-42) 639 32 18;
E-mail: [email protected]; Tel.: 0 507 151 972
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body against harmful impact of free radicals, different neutralizing molecules are
created. Among many chemical substances, enzymatic and non-enzymatic systems
are the most important in scavenging of free radicals. Those two systems constitute
what is known as the plasma oxidant capacity.
Enzymatic system in the human body plays a key defensive role against their
detrimental action. It consists of: superoxide dismutase, glutathione peroxidase and
catalase. Superoxide dismutase (SOD) exists inside the cells, e.g. in the cytosol and
mitochondria, as well as in plasma. In cytosol and in plasma there are forms of
SOD, which consist of copper and zinc: SOD 1 and SOD 3 (Cu, Zn SOD). In
mitochondria there is a form of SOD, which consists of manganese ions (Mn
SOD). All forms of SOD catalyze reaction of superoxide anion dismutation to
hydrogen peroxide:
O2-•+2H+ → H2O2+O2,
Glutathione peroxidase (GPx) occurs mainly in mitochondria and possesses
selenocysteine in its catalytic site. This enzyme is responsible for scavenging of
hydrogen peroxide and other organic peroxides:
2GSH + H2 O2
LOOH + 2GSH
GPx
GPx
GSSG + 2H2 O
LOH + GSSG + H2 O
Glutathione peroxidase requires glutathione as a substrate in the process of
peroxides decomposition. Oxidized glutathione is reduced by NADPH in the
presence of glutathione reductase:
GSSG + NADPH
+
2GSH + NADP
Another important enzyme is catalase, which decomposes hydrogen peroxide:
2H2O2
Cat
2H2O + O2
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The most relevant components of non-enzymatic system are: ascorbic acid
(vitamin C), ubichinon, taurine, glutathione, β-carotene, tocopherols (vitamin E),
albumin, uric acid, bilirubin and flavonoids. Glutathione is the most abundant
antioxidant in cytosol. Its concentration is much higher than other antioxidants
(1-2mM). GSH interacts with other low molecular weight antioxidants such as
ascorbic acid and α-tokoferol.
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Pentose
+ CO 2
GSSH
NADPH
a-TO
AH2
A
G-G-P
NADP
+
GSH
DHA
a-TOH
Glutathione can protect cellular components (protein and lipids) against
peroxidation initiated by hydroxyl radical or other radicals and reduces -S-Sbridges in oxidized protein:
.
GSH + Pr
.
GS + Pr H
2GSH + Pr
GSSG + Pr
SH SH
S S
Similar action in reduction of disulfides possesses thioredoxin. Ascorbic acid
effectively inhibits membrane lipid oxidation and helps recycle oxidized vitamin E.
Moreover, vitamin C can reduce lipid or protein radicals:
.
AH2 + R
-.
A +RH
Ascorbyl radical produces ascorbic and dehydroascorbic acid in the reaction of
disproportionation:
-.
+
2A
+ 2H
AH2 + DHA
In the reduction of dehydroascorbic acid to ascorbic acid glutathione plays
another important role:
DHA + 2GSH
GSSG +AH 2
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Plasma is composed of low molecular weight antioxidants such as ascorbic
acid, tocopherols (α,β,γ), β-caroten, and high molecular weight components such as
albumin, cerruloplasmin, ferritin, lactoferrin, which play an important role in
storing the transition metals, e.g. cooper and iron ions. Labile ions in reduced state
take part in Fenton or Haber-Weiss reactions, which lead to the generation of
hydroxyl radicals:
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H2 O2 + Fe2+
-.
H2 O2 + O2
.
Fe 3+ + HO + HO
.
O2 + HO + HO
Tocopherols and β-carotene, due to their lipophilic specificity, protect cell
membrane and plasma lipoproteins against oxidation. Diet components additionally
may have influence on antioxidant amount of non-enzymatic system
[1,2,18,29,36].
Currently, plasma antioxidant capacity is one of the most intensively
investigated scientific problems for many researchers and its diverse roles in cell
protection are proved [28]. In the existing literature, the role of plasma antioxidant
capacity in ageing processes as well as in different pathologies was presented in the
context of disturbance of antioxidant capacity components efficiency [29].
The aim of this article is a presentation of a current knowledge regarding the
changes of plasma antioxidant capacity observed in response to exercise as well as
in people with different level of physical activity and different health status.
1.2 Free radicals production
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During the past 20 years, the field of ‘free radical research’ has risen to become
a mainstream element of biomedical science. Chemically, a free radical is any
molecule containing a single, unpaired electron. Usually, paramagnetic transition
metal ions are not considered to be free radicals, although by technical definition
they are. An example of free radical is oxygen itself. It is a diradical with two
electrons, which are not spin paired, and each resides in an orbital of its own.
Unpaired electron is responsible for paramagnetic properties of free radicals and
their high reactivity toward molecules. Free radicals, which are metabolites of
oxygen biological systems, have diverse reactivity. For example, life-span of
hydroxyl radical OH• is t1/2=10-9s, whereas organic free radicals with delocalized
electron, like a melanin, are characterized by low reactivity and their t 1/2 equals a
few days [9]. From the chemical point of view, free radicals are active molecules
participating in chain reactions, in which free radical substrate leads to the
production of another free radical molecule, which in the another reaction gives the
product, which is a free radical as well. This process is defined as propagation of
free radicals reactions. Free radicals are therefore very unstable molecules with
variable reactivity. By obtaining electrons from the molecules situated nearby and
triggering a cascade of reactions, they can lead to the alteration of cellular structure
and inhibit activity of different enzymes.
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Free radicals are generated in numerous processes in living organisms. For
example in respiratory chain in mitochondria in the presence of coenzyme Q
reductase and NADH nicotinamide adenine dinucleotide, in microsome in the
presence of cytochrome P-450 reductase and endoplasmatic reticulum (cytochrome
P-450 reductase). Free radicals can be also generated in the membrane in presence
of lipoxygenase, or prostaglandine synthase.
Another source of free radicals is hemoglobin (Hb). During its oxidation to
methemoglobin (metHb) the superoxide anion radical is generated. During one day
3% of total mass of hemoglobin is converted to metHb. The most important source
of superoxide anion radicals is an electron transport chain. 85-90% of oxygen is
metabolized in mitochondria. One electron reduction of oxygen generates
superoxide anion free radical. Next stages of reduction lead to generation of
hydrogen peroxide and hydroxyl radicals:
O2
e
-. e
O2
H2 O2
e
.
OH
e
H2 O
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-
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However, most of oxygen (approx. 95%) is reduced to water molecules during
synthesis of ATP in mitochondria. In normal conditions, a man of weight 70 kg
uses 3.5 ml of O2/kg/min, which makes 350l O2/day (15 mol/day). It is assumed
that 2-3% of O2 is converted to superoxide anion radical (0.30-0.45 mol). During
extensive exercise the consumption of oxygen can increase by about 100%, so the
leakage of superoxide anion in respiratory chain can also be elevated by about
100%. An increase of superoxide anion is also possible during oxidation of
hemoglobin.
In healthy organisms free radical production and their inactivation by
antioxidative systems stay in equilibrium. Chapter 1 describes enzymatic and
nonenzymatic defensive systems in cells. When production of free radicals exceeds
cellular antioxidant capacity the oxidative injury occurs, which leads to the damage
of biological materials.
The main cellular components, which are susceptible to the activity of free
radicals, are unsaturated lipid acids, proteins, nucleic acids and carbohydrates. It is
believed that free radicals are generated in aging process and in all diseases.
However, these molecules can have different functions. They take part in the
regulation of many physiological processes, e.g. regulation of immunological and
enzymatic processes, oxidizing and reducing processes, gene transcription, as well
as in cellular signaling. Not much is still known, which process and which factor
establish boundaries between positive and detrimental functions of these molecules
in the body.
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Free radicals are divided into two different groups: reactive oxygen species
(ROS) and reactive nitrogen species (NOS). Reactive oxygen species include these
free radicals, which are formed in the reaction of molecular oxygen reduction as
well as these molecules, which are not free radicals but possess oxidative or
reductive properties. Due to uncompleted molecular oxygen reduction, the
generation of some of its reactive forms, named reactive oxygen species, takes
place in the cells. The family of reactive intermediates resulting from the
incomplete reduction of oxygen therefore includes: superoxide radical (O2-•),
hydrogen peroxide (H2O2), hydroxyl radical (HO•). These molecules are produced
under external factors like, for example, irradiation as well as under oxidative
process in the presence of oxydase and oxygenase or under nonenzymatic
autooxidations (e.g. catechole amine, thiol groups). Despite free radicals toxicity,
they play an important antimicrobial role through the phagocytes.
Nitric oxide (NO) with unpaired electron is a small, unstable, hydrophobic
molecule with a high diffusion coefficient and a short life-span. In spite of its
chemical properties connected with limited reactivity, this molecule can easily
react with hemoglobin, myoglobin, oxygen, superoxide anions, –SH groups of
proteins, and various cellular components. Nitric oxide properties allow the effect
of NO to occur close to its site of production. The reactions with molecular oxygen
and superoxide anions lead to the formation of reactive nitrogen species (RNS) like
nitrogen dioxide (NO2) and peroxynitrite (ONOO-). Peroxynitrite anion can be
transformed to peroxynitric acid, which decays by formation cytotoxic hydroxyl
radical and then nitrates are the final products of the reactions. Cellular damage
depends on the created factors involved in the reaction. Some of the created RNS
present higher reactivity with biological molecules than nitric oxide itself.
It was suggested that the major vascular pool of NO in vivo is nitrite, which is
present at concentrations of 0.5-10 µM in plasma, erythrocytes and tissues [19].
NO is synthesized from L-arginine by a family of isoenzymes called nitric oxide
synthases (NOSs). Depending on the concentration of NO in biological
environment, the effect of this molecule changes dramatically. Nitric oxide is
considered to be an endogenous modulator of numerous cellular functions in a
variety of tissues with properties of cell signalling molecule. It is also proven to be
a modulator of several aspects of skeletal muscle functions and, on the other hand,
a mediator of injury and disease. Lower concentration stimulates guanylate cyclase
and it influences blood pressure regulation, blood flow, neuronal transmission,
neuroendocrine activity [29]. In higher concentration, nitric oxide has
antimicrobial, antitumor and cytotoxic effect. Many diseases are also related to the
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over- and underproduction of NO and to the direct participation of NO in some
pathological mechanisms [7,8,45].
1.2 Methods used in the detection of free radicals during physical exhaustion
Concentration of free radicals in conjunction with the process of peroxidation
increases in some of the tissues due to physiological response of the body to
physical exhaustion. Biochemical measurements of the level of generated free
radicals are mainly based on indirect assessments of oxidative stress. These
methods use only co-products detection of free radicals reactions.
More sophisticated method, which can be utilized in exercise physiology and
medicine, is electron paramagnetic resonance (EPR). EPR allows for direct
detection of free radicals in physiological and biochemical systems. For many
researchers EPR technique is known as the most specific, sensitive and direct
method for measuring free radicals [4,13,20]. It was demonstrated that free radicals
production detected by EPR in the circulation is connected with extracellular
hydroxyl radical production [4,20]. Moreover, it is believed that detecting of the
circulating EPR radical provides a non-invasive method of evaluation hydroxyl
radical generation in skeletal muscle [4,20].
Spin trapping method is used to transform short life radicals to the stable
paramagnetic adduct, which can be measured in room temperature. The reaction of
free radical with spin trap is as follows:
.
R1 N CH R2 + R
-
O
R1 N CH R2
.
O
R
-
-
-
-
-
where R can be hydroxyl radical, superoxide, alcoxyl, or peroxide radical.
EPR in conjunction with spin trapping method was applied in the investigation
of maximal physical exhaustion (with the usage of cycle ergometer) according to
progressive and incremental exercise protocol [4,5]. Studies showed a statistically
significant increase of EPR signal intensity, which derived from tert-butylnitrone
(PBN) adducts after exercise [4,5]. Spectrum analysis in both studies showed that
alcoxyl radical was generated during oxidative damage of membrane lipids. It can
be explained by the fact that lipid peroxidation is a chain reaction, which in
consequence leads to the free radicals formation. Authors presented three-fold
increase of the free radicals concentration after exercise [4]. The highest elevation
was detected among the subjects with the highest maximal oxygen uptake
(VO2max). Furthermore, a statistically significant increase of lipid peroxidation as
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well as total antioxidant capacity (TAC) was observed [4]. Another study was
performed with healthy volunteers, who for 8 weeks before entering the
investigation were supplemented with 1000 mg of ascorbic acid [5]. Results were
compared with the subjects without vitamin C supplementation. Volunteers were
subjected to a single bout of exhaustive exercise. EPR analysis presented a
significant increase of signal intensity, which derived from PBN adduct
immediately after exercise. This was connected with the process of free radicals
production. EPR signal intensity was correlated with free radicals concentration in
the sample. Spectra analysis as well as comparison of hyperfine coupling constants
recorded from EPR suggested that trapped free radical was alcoxyl radical derived
from the reaction between oxygen-centered radicals with membrane phospholipids.
EPR signal intensivity after exercise in supplemented subjects was similar to
control samples before exercise. Ascorbic acid appeared to be a very efficient
antioxidant. Results from this study suggest that the supplementation of high
dosage of vitamin C significantly influences the decrease of EPR signal intensity as
well as inhibits lipid peroxidation. A diet rich in vitamin C can effectively protect
body against reactive species production induced by physical exhaustion. However,
overdosing of the vitamin C is not neutral for the body. Therefore, high dosages of
this vitamin are nowadays not recommended [13]. Results described by Asthon et
al. [4,5] were confirmed by the experiment from another study [13], in which EPR
technique was similarly used for direct free radicals assessment. Hyperfine
coupling constants analysis revealed that alcoxyl radical was trapped and derived
from the membrane lipids peroxidation. In this study also copper-derived radical
was detected. It can suggest the albumin deterioration upon physical exhaustion. A
significant increase of reactive oxygen species was observed following downhill
running occurred 72 h post exercise. Furthermore, this increase in ROS production
occurred at a time when the peak of muscle soreness decreased and muscles
functions returned to the baseline values. This may suggest that ROS are not
responsible for initiating the damage but may play role in mediating the recovery.
Based on the existing literature, EPR in conjunction with spin trapping method
in physiological model of oxidative stress generated by physical exercise can be
utilized in this research area and can be recognized as the direct and specific
assessment of free radicals.
The biochemical method, which is commonly used in the investigation of
oxidative stress, is the indirect markers analysis of lipid peroxidation like
malondialdehyde (MDA), diens, expired pentane, lipid hydroperoxides, conjugated
diens, isoprostanes. Most studies have used MDA as a measure of oxidative stress
imposed by exercise. Generated free radicals can attack membrane polyunsaturated
Antioxidant capacity and physical exercise
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lipids acids and develop process of lipid peroxidation. The most common indirect
detection of generated oxidative stress to assess changes in MDA with exercise is
the thiobarbituric acid (TBARS) assay. TBA can react with several aldehydes to
form yellow or orange complexes. Santos-Silva et al. [38] described increase of
resting MDA level in trained adolescent swimmers compared with control subjects.
Also Marzatico et al. [33] found higher MDA level in marathon runners compared
with subjects. Several studies showed that single bout of exercise increase blood
level of MDA [21,34]. However strenuous endurance training was shown to reduce
indices of oxidative stress [34]. Moreover, in response to exercise in trained skiers
and runners immediately after the exercise the decrease of MDA was presented
[23,37]. Despite the fact that this method is widely used in the sport science for
lipid membrane peroxidation, the method itself and the obtained results are
questioned in the existing literature. It is a matter of discussion whether the
discrepancies between different studies are within acceptable limits, and it seems
that some of the reported values may not reflect true levels of thioarbituric acid
reactive substances (TBARS) in vivo. Criticism of this method is mainly connected
with lack of specificity and repeatability [27]. Diversity of the results interpretation
may be connected with different modifications of the method by many authors
[20,30,32]. One reason why no significant amounts of MDA are detected using
classical method is that MDA binds to proteins [11]. To detect free and bound
MDA the TBARS-assay has been modified to realise protein-bound MDA, which
can be achieved by hot alkali digestion [16]. However spectrophotometric spectra
analyses show the lack of specificity of TBA in binding aldehydes.
Glutathione is another important marker of oxidative stress. It plays an
important role in the elimination of organic peroxide and hydroxide peroxide. The
GSH-GSSG ratio decreases under oxidative conditions. To detect both forms of
glutathione HPLC and spectrophotometric techniques can be applied. Some studies
presented that blood GSSG and GSH-GSSG ratio decreases in response to exercise
[39,41]. Recently it has been suggested that oxidatively modified hemoglobin
(OxHm) may be useful as an indicator of a specific form of oxidative stress, more
than described above lipid peroxidation and glutathione redox status. Vollaard et
al. [49] demonstrated that in vivo oxidative modification to haemoglobin is a
normal occurrence in human blood, and is enhanced by exercise. Due to the fact
that OxHm is produced in erythrocytes by peroxidation of haemoglobin, the
changes in its concentration may provide direct mechanistic and diagnostic
information.
In the response of the body to physical exercise, the changes in plasma
antioxidant capacity can be analyzed based on the model of experimental exercise
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test. All applied model exercise tests are very simple and repeatable. During a
single bout of exercise the basic hemodynamic factors are changed, e.g. the
increase of heart contractions frequency, systolic blood pressure, and minute
volume of the heart [26]. During the performance of such a test it is possible to
estimate physical capacity of the body as well as VO2max [29].
Physical exhaustion induces production of free radicals in different ways. The
level of oxidative phosphorylation increases, which is responsible for ATP
production. This reaction as a response of the body to physical exhaustion is
connected with free radical production. Also exercises performed on the regular
basis induce elevation of oxygen uptake, which is correlated with 10 up to 20-fold
higher increase of cellular metabolism and with intensive oxygen radicals
production.
Problems, which appear in interpretation of the results of various studies, are
mainly connected with different procedures according to which they were
performed. Authors describe changes in enzymatic and non-enzymatic
environments after single bout of exercise with the usage of cycle ergometer as
well as after long term exercise like marathon or mountain cycling. Another reason
for the discrepancies in results interpretation is a difference in used methodologies
as well as a variety of substances, which are applied in the detection of the
alterations in the body.
1.4 Antioxidant capacity in people with regular physical activity
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Changes of enzymes activity under physical exhaustions in regularly trained
subjects are ambiguous.
Analysis of superoxide dismutase activities showed contradictory results. Some
studies showed that SOD activity increased during exercise tests performed on
cycle ergometer or treadmill [10,40,46], but no significant changes among cyclists
were detected [6]. However a decrease during exercise on cycle ergometer was
described by Groussard [20].
Glutathione peroxidase level increased significantly after exercise tests with the
usage of treadmill and cycle ergometer [29,40,46]. However tests where
participants were subjected to maximal exhaustion within the next 5 days the
decrease of enzyme concentration was observed. Return to the baseline level was
observed 3h after performance of physical test. However glutathione concentration
measured in the same time did not confirm results obtained for glutathione
peroxidase concentration. Tests performed on cycle egrometer presented a decrease
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of glutathione concentration [20,46], whereas other tests (sport exercises) showed
an increase of glutathione concentration [24,29].
Results from catalase activity are more univocal. Analyses of results revealed
an increase of its activity under physical exhaustion [6,29,46], or no statistically
significant difference after exercise [40].
Creatine kinase activity mostly increased immediately after exercise test
[12,29,31]. However no statistically significant difference among people with
regular physical activity was observed. It can support the theory of muscle cells
damage after exercise [29]. Some of investigations indicate a higher level of kinase
concentration at rest in trained people [29].
Only few studies focused on alterations of non-enzymatic system of antioxidant
capacity. Some reports presented an increase of tocopherol and ascorbic acid
[6,10,29]. However results obtained from weight lifting women were contradictory
[31]. Also in cyclists no differences in concentration of retinol and β-carotene were
detected [6].
Regardless of the existing differences in reported results, various studies tend to
indicate a significant impact of physical exercise on free radicals production. It
may be necessary to pay more attention on individual total antioxidant capacity in
physical training planning.
1.5 Antioxidant capacity in people with low physical activity
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Interpretation of results concerning people with the so-called sedentary lifestyle
is difficult because there exist very few studies, which are focused particularly on
that group. Usually subjects characterized by low physical activity are used as
control group.
In many studies the analysis of total antioxidant capacity level shows that its
initial value is lower in untrained group than in the trained one [10,17,40]. Exercise
tests or series of training allow for conclusions that level of total antioxidant
capacity increases in group without regular physical activity [15,17,40].
It was demonstrated that SOD concentration increases after physical exhaustion
[15,40]. Similar effect was observed in case of glutathione peroxidase [40].
However results from the same study showed that concentration of both enzymes
was lower in subjects with low physical activity than in the trained group. Using
cycle egrometer in the sedentary patients the level of reduced glutathione decreased
immediately after physical exhaustion, but it significantly increased in recovery
[25]. Similarly, there was no difference in catalase activity after exercise test [40].
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Another study performed among volunteers with low physical activity (with the
usage of cycle ergometer) showed the results from indirect detection of ROS
production with the application of TBARS assay. The concentration of
thiobarbituric acid reactive substances increased during exercise with the
maximum level in recovery. Positive correlation between TBARS value in
recovery and the subject’s age was found. The older the subject, the higher the
TBARS value was estimated [25].
Components of non-enzymatic system were investigated during exercise in
studies with group of low physical activity. Few of them indicated the decrease of
ascorbic acid concentration [25] and no changes in tocopherol level [14].
In other studies, the changes of lipid peroxidation in blood plasma were
analysed (mainly HDL and LDL cholesterol fraction). No statistically significant
influence of physical exhaustion on lipid peroxidation in group with sedentary
patients was detected [14,40].
Due to the fact that people with sedentary lifestyle have lower total antioxidant
capacity, it may be necessary to plan and increase the intensity of physical
exercises more carefully, so that human body can adapt defensive mechanisms to
the increased production of free radicals.
1.6 Antioxidant capacity during physical exhaustion in people with
cardiovascular diseases
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Oxidative stress can cause changes in function of endothelial lining of internal
side of blood vessels. Endothelium is responsible for vessel function, it secretes
substances regulating gases and chemical substances transport as well as hormones
and molecules determining vessel contraction (e.g. nitric oxide). Aerobic exercise
exacerbates oxidative stress, which is connected with an increase of lipid
peroxidation, which significantly induces processes of atherosclerosis inside blood
vessels [35,43]. On the other hand it is well known that exercise performed on
regular basis supports angiogenesis and arteriogenesis, improves tissues blood flow
and activates intracellular defence mechanisms against atherosclerosis evolution.
Regular physical activity is related to antiapoptotic and fibroblasts antiproliferation
activities. It also increases availability of nitric oxide, which improves diastolic
reaction on elevated blood pressure [28]. Antioxidant system protects generated
nitric oxide and enables its more efficient use [22].
Existing studies about efficiency of supplementation with ascorbic acid and
tocopherol in cardiovascular diseases indicate favourable decrease of lipid
peroxidation as well as positive increase of total antioxidant capacity [22,47].
Antioxidant capacity and physical exercise
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In subjects with arterial hypertension a higher level of oxidative stress in rest
and during physical activity is reported. In that group the lower activity of
superoxide dismutase and catalase was detected comparing to healthy subjects.
Furthermore, the increase of oxidative damage protein products was reported after
physical exercise [44].
In subjects with coronary heart disease an increase of superoxide dismutase and
glutathione peroxidase activity was detected. The level of oxidized LDL molecules
in blood serum also was higher in rest [50]. It may indicate that this group of
patients is characterized by increase of chronic oxidative stress despite medical
treatment and lack of clinical symptoms. However other experiments showed a
decrease of glutathione peroxidase, superoxide dismutase and glutathione with a
significant increase of TBARS level in patients with coronary heart disease after
exercise test [3]. Similar results were obtained in group of patients with myocardial
infarction after cardiogenic shock complications. A decrease of antioxidant
enzymes activity in blood serum and in concentration of ascorbic acid, tocopherol
and β-carotene were observed [42].
Results published in existing literature indicate an important role of antioxidant
capacity components in pathogenesis of cardiovascular diseases and their
evolution. Results interpretation and comparison with healthy population has to be
done with particular attention to differences connected with changes in antioxidant
capacity related to the age of examined subjects and also to their pharmacological
treatment. It should be additionally considered that physical exercise performed by
people with cardiovascular diseases, in secondary prevention as well as in assisting
treatment, can also change antioxidant capacity of blood plasma.
1.7 Summary
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The described results from different studies indicate that the role of components
of antioxidant capacity is not well established, especially in the context of exercise
performed by patients in different clinical states or in subjects with different
physical activities. Various methods, which are applied in antioxidant capacity
investigations as well as various exercise protocols do not allow for making an
univocal statement about a profile of changes, which occur in the human body
upon physical exhaustion. We would like to suggest that planning the intensity of
physical activity in healthy subjects with different exercise level and in patients
with diseases, the individual scavenging and protecting ability of the body against
detrimental influence of free radicals should be carefully analyzed. Therefore we
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would like to emphasize that antioxidant capacity should be considered in the
patients classification to physical effort.
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Accepted for publication 21.02.2008
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Supported by KBN grant N N404 1067 33